Stanford team links macrophage EP2 receptor to multi-organ aging in mice

Stanford Medicine researchers report that blocking a single inflammatory receptor on tissue-resident macrophages protected mice from many aging effects across organs, SciTechDaily reported on a Science paper. The team traced cleanup failure to long-lived macrophages that dispose of dead, damaged and aging cells. As those cells lose clearance capacity, inflammatory debris accumulates. Blocking one receptor, known as EP2, preserved function in brain, heart, liver, kidneys, colon, spleen, bone marrow and skeletal muscle. Mice with the receptor selectively disabled developed less frailty, accumulated less fat, retained more muscle, and performed better on memory, balance, strength and organ tests, with fewer signs of persistent inflammation. Katrin Andreasson, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences, said the work addresses why organisms age and identifies at least one major reason. The study points to a shared immune source for multi-organ decline rather than independent aging in each tissue. The paper, "Restored clearance of senescent neutrophils by tissue-resident macrophages limits organ aging" by Yuting Jessy Tan and colleagues, lists publication as 16 July 2026 in Science with DOI: 10.1126/science.aea3075. SciTechDaily said the study was funded by the National Institutes of Health (grants 1RF1AG080742, 1RF1AG070839 and P30AG066515), the American Heart Association, the Phil and Penny Knight Initiative for Brain Resilience (at the Wu Tsai Neurosciences Institute), Stanford University, the Arc Institute, and the Chan-Zuckerberg Biohub.